Understanding the neural mechanisms of motivation will provide relevant knowledge for the development of therapies for a number of maladies like obesity, anorexia nervosa, and depression. A change in the significance of sensory neural activity is a defining feature of motivated behavior. In most mammals, including humans, a negative sodium balance triggers the biological drive termed salt appetite and changes dramatically the significance of neural activity elicited by sodium salt. It is known that the behavioral expression of a salt appetite is coincident with alterations in the responsiveness of brain stem neurons to sodium salt. One interpretation of this modulation in response to visceral signals is that descending forebrain input normally regulates taste processing in the brain stem. This is supported by the fact that chronically decerebrate rats fail to express a salt appetite. The research in this application investigates the influence of descending input from the central nucleus of the amygdala (CeA), the lateral hypothalamus (LH), and the gustatory cortex (GC) on taste-evoked responses in the parabrachial nucleus (PBN). These central nuclei receive both gustatory and visceral sensory information and are of import to the elaboration of taste-guided motivated behavior. Anatomically, these rostral brain structures are reciprocally connected with each other and with the PBN. Prior studies have shown that electrical stimulation in the LH and GC modulated the ongoing activity in brain stem taste cells; however, the effects on gustatory-evoked responses and the potential convergence of different sources of descending input have not been assessed. Our own initial study, in acutely prepared rats, demonstrated that descending input from the CeA sharpened the response functions of many PBN taste cells. The present experimental procedure affords the opportunity to use less anesthesia and to collect data from each animal over several recording sessions. The proposed study will establish whether the CeA is unique in terms of its ability to modulate gustatory sensory processing in the PBN. If not, as we predict, are the same neurons influenced by centrifugal input from the CeA, LH, and GC, and in the same way?